Interspecies platelet immunizations among marmosets (S. oedipus, S. fuscicollis, and C. jacchus) invariably lead to thrombocytopenia and antibody development toward the donor (but not host) platelet elements. The clinical and physiologic manifestations of this disease closely resemble that observed in posttransfusion purpura in man, a hematologic disorder falling within the syndrome of idiopathic thrombocytopenic purpura. The dose of platelets, route of injection, and suspending vehicle are critical variables in determining the time of onset and severity of the induced disease. The mechanism of destruction of host platelets is not known although current evidence points to deposition of an antigen-antibody complex on these elements which are then readily eliminated through the reticuloendothelial system. A key observation supporting this concept in this animal model has been the deposition of IgG on the animal's platelets following immunization and prior to the onset of thrombocytopenia. Whether this is part of an antigen-antibody complex is yet to be discerned. Attempts to show the in vitro development of cytotoxic (to platelet antigens) lymphocytes following their exposure to such IgG-coated platelets have been negative. In a few animals we have now been able to maintain a state of IgG ion platelets in the absence of thrombocytopenia. Platelet survival studies suggest a rapid turnover of platelets in these animals rather than the existence of serum factors protecting them from destruction.